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致癌物诱导胚胎蛋白合成的理论机制:X. 肝癌的诱导性与甲胎蛋白基因活性的相关性。

Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: X. Correlation of the induceability of hepatomas and alpha-fetoprotein gene activity.

作者信息

Payette R, Hancock R L

出版信息

Med Hypotheses. 1982 Oct;9(4):429-35. doi: 10.1016/0306-9877(82)90083-4.

Abstract

We have observed a distinct difference in the alpha-fetoprotein production of Sprague-Dawley rats and Swiss white mice. When both animals are fed a 1% D/L-ethionine diet, only the rat responds with increased levels of hepatic alpha-fetoprotein synthesis as shown by radioimmunoassay studies. Also, hybridization studies, with a complementary deoxyribonucleic acid for alpha-fetoprotein messenger ribonucleic acid, proved negative for the mouse, even after forty days on the 1% D/L-ethionine diet. This evidence, combined with other information leads us to believe that the mouse has a genomic regulatory system that is resistant to carcinogenic change by certain chemicals. Furthermore it may eventually be proven that hepatic tissue that is competent to have certain embryonic genes activated may also be capable of becoming neoplastic.

摘要

我们观察到斯普拉格-道利大鼠和瑞士小白鼠在甲胎蛋白产生方面存在明显差异。当给这两种动物喂食1%的D/L-乙硫氨酸饮食时,通过放射免疫分析研究表明,只有大鼠肝脏甲胎蛋白合成水平会升高。此外,用甲胎蛋白信使核糖核酸的互补脱氧核糖核酸进行杂交研究,结果显示即使在喂食1%的D/L-乙硫氨酸饮食40天后,小鼠的检测结果仍为阴性。这些证据,再结合其他信息,使我们相信小鼠具有一种基因组调节系统,该系统对某些化学物质引起的致癌变化具有抗性。此外,最终可能会证明,能够激活某些胚胎基因的肝脏组织也可能会发生肿瘤。

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